title: Reversal of mitochondrial dysfunction by coenzyme Q10 supplement improves endothelial function in patients with ischaemic left ventricular systolic dysfunction: a randomized controlled trial.
abstract: OBJECTIVE
  Coronary artery disease (CAD) is associated with endothelial dysfunction and mitochondrial dysfunction (MD). The aim of this study was to investigate whether co-enzyme Q10 (CoQ) supplementation, which is an obligatory coenzyme in the mitochondrial respiratory transport chain, can reverse MD and improve endothelial function in patients with ischaemic left ventricular systolic dysfunction (LVSD).
  
  
  RESULTS
  We performed a randomized, double-blind, placebo-controlled trial to determine the effects of CoQ supplement (300 mg/day, n=28) vs. placebo (controls, n=28) for 8 weeks on brachial flow-mediated dilation (FMD) in patients with ischaemic LVSD(left ventricular ejection fraction <45%). Mitochondrial function was determined by plasma lactate/pyruvate ratio (LP ratio). After 8 weeks, CoQ-treated patients had significant increases in plasma CoQ concentration (treatment effect 2.20 μg/mL, P<0.001) and FMD (treatment effect 1.51%, P=0.03); and decrease in LP ratio (treatment effect -2.46, P=0.03) compared with controls. However, CoQ treatment did not alter nitroglycerin-mediated dilation, blood pressure, blood levels of fasting glucose, haemoglobin A1c, lipid profile, high-sensitivity C-reactive protein and oxidative stress as determined by serum superoxide dismutase and 8-isoprostane (all P>0.05). Furthermore, the reduction in LP ratio significantly correlated with improvement in FMD (r=-0.29, P=0.047).
  
  
  CONCLUSIONS
  In patients with ischaemic LVSD, 8 weeks supplement of CoQ improved mitochondrial function and FMD; and the improvement of FMD correlated with the change in mitochondrial function, suggesting that CoQ improved endothelial function via reversal of mitochondrial dysfunction in patients with ischaemic LVSD.
authors.affiliation: Cardiology Division, Department of Medicine, The University of Hong Kong, Hong Kong.
authors.forename: Yuk-Ling
authors.initials: YL
authors.lastname: Dai
authors.forename: Ting-Hin
authors.initials: TH
authors.lastname: Luk
authors.forename: Kai-Hang
authors.initials: KH
authors.lastname: Yiu
authors.forename: Mei
authors.initials: M
authors.lastname: Wang
authors.forename: Pandora M C
authors.initials: PM
authors.lastname: Yip
authors.forename: Stephen W L
authors.initials: SW
authors.lastname: Lee
authors.forename: Sheung-Wai
authors.initials: SW
authors.lastname: Li
authors.forename: Sidney
authors.initials: S
authors.lastname: Tam
authors.forename: Bonnie
authors.initials: B
authors.lastname: Fong
authors.forename: Chu-Pak
authors.initials: CP
authors.lastname: Lau
authors.forename: Chung-Wah
authors.initials: CW
authors.lastname: Siu
authors.forename: Hung-Fat
authors.initials: HF
authors.lastname: Tse
mesh_terms: D000368:Aged; D001794:Blood Pressure; D001916:Brachial Artery / Q000473:pathology; D003430:Cross-Sectional Studies; D019587:Dietary Supplements; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D005996:Nitroglycerin / Q000378:metabolism; D010919:Placebos; D012307:Risk Factors; D013482:Superoxide Dismutase / Q000097:blood; D014451:Ubiquinone / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000473:pathology
chemical_list: D010919:Placebos; D014451:Ubiquinone; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D013482:Superoxide Dismutase; C024989:coenzyme Q10; D005996:Nitroglycerin